Insulin's action on mammalian cells appears to involve regulation of a number of vital metabolic processes and functions, such as, glucose transport and utilization, and activation of the biosynthesis pathways leading to fatty acid synthesis and storage as acylglycerols, and protein synthesis and antagonizing fatty acid mobilization. These variety of metabolic effects, termed "the pleiotypic effects" are subject to a renewed investigation, since we first demonstrated that insulin's effects on glucose oxidation or antagonism of adenylate cyclase activity are regulated by a mechanism distinct from the activation of D-glucose transport. This is in concert with the recent reports that many important biological effects of insulin are independent of glucose translocation. Although the hormone reacts exclusively on the specific cell-surface receptors, it may generate a single or multiple messenger molecules to regulate the separate metabolic pathways within the cells. Previous attempts to identify any messenger system for this hormone were not successful. We have recognized an oxidase activity in the plasma membrane of the target cells, the adipocytes, which responds to insulin and leads to a drastic change in the cytoplasmic redox state. Our present aim is to identify, isolate and characterize the reaction cycle within the plasma membrane and in the cytoplasm which are triggered, subsequent to the hormone-receptor binding, and to correlate these functions to the known loci of insulin-mediated reactions within the cells. Adipocytes are the most convenient model system for these studies. We believe that identification and characterization of the reactive plasma membrane components and of their product(s) may finally elucidate the mechanism of action of this hormone and the molecular changes leading to insulin-resistance. This should further help exploring experimental conditions to reverse these disease states.